MATERNAL OBESITY, METABOLISM, AND
PREGNANCY OUTCOMES
Janet C. King
Children’s Hospital Oakland Research Institute, the University of California at Berkeley,
and the University of California at Davis, Oakland, California 94609;
email: [email protected]
KeyWords pregnancy, fetus, nutrition, obesity, gestational diabetes
■ Abstract About one third of all pregnant women in the United States are obese.
Maternal obesity at conception alters gestational metabolic adjustments and affects
placental, embryonic, and fetal growth and development. Neural tube defects and
other developmental anomalies are more common in infants born to obese women;
these defects have been linked to poor glycemic control. Preeclampsia, a gestational
disorder occurring more frequently in obese women, appears to be due to a subclinical
inflammatory state that impairs early placentation and development of its blood
supply. Fetal growth and development during the last half of pregnancy depends on
maternal metabolic adjustments dictated by placental hormones and the subsequent
oxygen and nutrient supply. Maternal obesity affects these metabolic adjustments as
well. Basal metabolic rates are significantly higher in obese women, and maternal
fat gain is lower, possibly in response to altered leptin function. The usual increase
in insulin resistance seen in late pregnancy is enhanced in obese mothers, causing
marked postprandial increases in glucose, lipids, and amino acids and excessive fetal
exposure to fuel sources, which in turn increases fetal size, fat stores, and risk for disease
postnatally. Impaired glucose tolerance, gestational diabetes, and hyperlipidemia
are more common among obese mothers. To date, little attention has been given to
the role of diet among obese women in preventing these problems. However, studies
of women with impaired glucose tolerance show that replacing refined carbohydrates
and saturated fat with complex, low-glycemic carbohydrates and polyunsaturated fatty
acids improves metabolic homeostasis and pregnancy outcomes. Thus, current dietary
guidelines regarding the amount and type of carbohydrates and fat for nonpregnant
women seem appropriate for pregnant women as well.
CONTENTS
INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
EMBRYONIC DEVELOPMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273
Embryonic and Placental Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273
Aberrations in Embryonic and Placental Development . . . . . . . . . . . . . . . . . . . . . . . 274
METABOLISM DURING LATE PREGNANCY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
Energy Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
0199-9885/06/0821-0271$20.00 271
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272 KING
Fuel Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
FETAL GROWTH AND DEVELOPMENT IN LATE PREGNANCY . . . . . . . . . . . . 282
MATERNAL DIET AND PREGNANCY OUTCOMES . . . . . . . . . . . . . . . . . . . . . . . 283
Dietary Carbohydrate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 284
Dietary Fat . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 284
Diet Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285
PERSPECTIVES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285
INTRODUCTION
Coincident with the rise in obesity nationwide, the number of women who enter
pregnancy obese has reached an all-time high. Based on the prevalence of obesity
among women of reproductive age, it appears that at least one third of all pregnant
women in the United States are obese. Data from the Centers for Disease Control
and Prevention collected in 2000 show that 50% of African American women
40% of Hispanic women, and 30% of white women are obese. Many studies of
thin, undernourished women have shown that maternal nutrition at conception influences
the metabolic response to pregnancy and fetal growth and development
(68). Undernourished women gain less weight, have smaller increases in basal
metabolism, and give birth to smaller babies. But the number of studies of pregnancy
outcomes among women who enter pregnancy with excessive amounts of
fat stores is more limited. As the prevalence of obesity increases, however, it is becoming
evident that these women are susceptible to an increased risk of metabolic
complications and poor pregnancy outcomes (18, 29, 37). Fetal anomalies as well
as deviations in fetal growth rates are more common among obese compared with
normal-weight women, suggesting that maternal adiposity affects development
during both the embryonic period as well as later in gestation. The intrauterine
effects on fetal growth and development may also affect postnatal development of
the child, particularly if fetal growth rates are abnormal. Large-for-gestational age
(LGA) infants are at increased risk for childhood obesity, which can lead to insulin
resistance, diabetes, and hypertension later in life (21). Small-for-gestational
age (SGA) infants born to obese women are susceptible to cardiovascular disease
and diabetes later in life, particularly if their postnatal catch-up growth produces
truncal obesity but the child remains short (89, 92).
Two factors influence fetal growth and development—genetics and the maternal
environment (38). Although genetics influences intrauterine growth rates
and development of fetal anomalies, it is unlikely that the increased prevalence
of fetal complications among obese mothers is due to genetics alone. It is more
likely that the environment of obese mothers interacts with genetic factors to induce
changes in fetal growth and development. The fetus perceives the maternal
environment through signals transmitted by the placenta, such as nutrient transfer,
blood hormone, or oxygen levels. The fetus uses this information in two ways:
(a) to make immediate survival choices and (b) to make longer-term adjustments
to maximize its advantage postnatally (38). For example, if blood oxygen levels
Annu. Rev. Nutr. 2006.26:271-291. Downloaded from www.annualreviews.org
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MATERNAL OBESITY 273
drop, fetal growth rates slow to conserve oxygen. On the other hand, if the fetus
experiences a chronically high blood glucose level, it might anticipate being born
into a carbohydrate-rich environment and prepare for that situation by synthesizing
and secreting more insulin.
Environmental signals to the fetus from obese mothers that influence fetal development
include adjustments in the placental transfer of nutrients (e.g., glucose,
fatty acids, amino acids), hormones (e.g., insulin, leptin, adiponectin), and, possibly,
inflammatory markers. When these metabolic parameters reach abnormal
levels, metabolic complications such as gestational diabetes, pregnancy-induced
hypertension, and preeclampsia are diagnosed. Although it is well known that diet
influences the development of diabetes and hypertension in nonpregnant adults,
the role diet plays in either prevention or management of these disorders among
obese pregnant women has received little attention. Consequently, obese women
are not given any special prenatal dietary counseling unless they develop gestational
diabetes. It is important to know whether adjustments in maternal diet either
prior to and/or during gestation improve outcomes among obese women.
This review summarizes the effects of maternal adiposity on placental function
and fetal growth and development. Differences in the metabolic adjustments and
complications among obese compared with nonobese women are examined and
linked, to the extent possible, to pregnancy outcomes. Finally, the potential role
of maternal diet, an important aspect of the maternal environment, in influencing
gestational metabolic adjustments is discussed.
EMBRYONIC DEVELOPMENT
Embryonic and Placental Development
Human pregnancies are usually divided into two stages of development—
embryonic and fetal (38). During the embryonic period, or the first 14 weeks
of gestation, gross development of the fetal anatomical features and placental formation
occur. The remaining 26 weeks of gestation are devoted to completing fetal
growth and development. Prior to implantation, the blastocyst becomes polarized,
with one part becoming the embryo and another part forming the placenta. As the
cells destined to become the placenta proliferate, they invade the uterine lining and
establish contact with maternal blood vessels so that the growing embryo can be
nourished (38).
Embryonic
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